Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
The secretory proprotein convertase neural apoptosis-regulated convertase 1 (NARC-1): liver regeneration and neuronal differentiation.
Functional characterization of Narc 1, a novel proteinase related to proteinase K.
Hepatic PCSK9 expression is regulated by nutritional status via insulin and sterol regulatory element-binding protein 1c.
The proprotein convertase (PC) PCSK9 is inactivated by furin and/or PC5/6A: functional consequences of natural mutations and post-translational modifications.
Proapoptotic effects of NARC 1 (= PCSK9), the gene encoding a novel serine proteinase.
Secreted PCSK9 decreases the number of LDL receptors in hepatocytes and in livers of parabiotic mice.
A novel loss of function mutation of PCSK9 gene in white subjects with low-plasma low-density lipoprotein cholesterol.
Degradation of the LDL receptors by PCSK9 is not mediated by a secreted protein acted upon by PCSK9 extracellularly.
Binding of proprotein convertase subtilisin/kexin type 9 to epidermal growth factor-like repeat A of low density lipoprotein receptor decreases receptor recycling and increases degradation.
The cellular trafficking of the secretory proprotein convertase PCSK9 and its dependence on the LDLR.
The proprotein convertase PCSK9 induces the degradation of low density lipoprotein receptor (LDLR) and its closest family members VLDLR and ApoER2.
Self-association of human PCSK9 correlates with its LDLR-degrading activity.
Annexin A2 is a C-terminal PCSK9-binding protein that regulates endogenous low density lipoprotein receptor levels.
Mechanistic implications for LDL receptor degradation from the PCSK9/LDLR structure at neutral pH.
Regulation of epithelial sodium channel trafficking by proprotein convertase subtilisin/kexin type 9 (PCSK9).
Proprotein convertase subtilisin/kexin type 9 interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor.
Insights into RNA biology from an atlas of mammalian mRNA-binding proteins.
Annexin A2 is a natural extrahepatic inhibitor of the PCSK9-induced LDL receptor degradation.
Annexin A2 reduces PCSK9 protein levels via a translational mechanism and interacts with the M1 and M2 domains of PCSK9.
MMP-2 inhibits PCSK9-induced degradation of the LDL receptor in Hepa1-c1c7 cells.
PCSK9:LDLR:Clathrin-coated vesicle transport from plasma membrane to endolysosome
PCSK9:LDLR bind to Clathrin
Degradation of PCSK9:LDLR:Clathrin-coated vesicle
VLDLR:PCSK9:Clathrin-coated vesicle translocates from the plasma membrane to lysosomal membrane
VLDLR:PCSK9 binds Clathrin-coated vesicles
FAM20C phosphorylates FAM20C substrates
PCSK9 binds PCSK9 inhibitors